Etiology African Horse Sickness S Epidemiology African ... · African Horse Sickness ... virus (AHSV), a non-enveloped, double-stranded RNA virus from the family ... morphology and

African Horse Sickness

Center for Food Security and Public Health 2012 1

Slide 1


Perdesiekte,

Pestis Equorum,

La Peste Equina,

Peste Equina Africana

African horse sickness (AHS), also known as Perdesiekte, Pestis Equorum,

La Peste Equina, and Peste Equina Africana, is a serious, often fatal,

disease that affects members of the Equidae family. The disease is spread

by arthropod vectors (primarily Culicoides species– biting midges), with

mortality in horses as high as 95%. Currently the disease is endemic in

Africa, however infected animals or vectors may carry the virus into AHS-

free regions. AHS is considered as one of the most lethal of horse diseases

and is an OIE reportable disease (http://www.oie.int/animal-health-in-the-

world/oie-listed-diseases-2011/).

Slide 2

Overview

• Etiology

• Species Affected

• Epidemiology

• Economic Importance

• Clinical Signs

• Diagnosis and Treatment

• Prevention and Control

• Actions to TakeCenter for Food Security and Public Health, Iowa State University, 2011

This presentation will discuss African horse sickness, its etiology, species

affected, and transmission. It will also cover the epidemiology (e.g.,

geographic distribution, morbidity, mortality) of the disease as well as

outline the economic impact the disease has had in the past and could have

in the future. Additionally, we will overview the clinical signs and

necropsy findings, as well as the diagnosis and treatment of the disease.

Finally, we will address prevention and control measures for the disease,

as well as actions to take if AHS is suspected.

[This photo shows a horse standing in a field. Source: www-flickr-

com_creative-commons]

Slide 3

ETIOLOGY

Center for Food Security and Public Health, Iowa State University, 2011

Slide 4

African Horse Sickness Virus

• Non-enveloped RNA

• Family Reoviridae–Genus Orbivirus

• Nine serotypes (1-9)–All viscerotropic

–Serotype 9• Endemic areas

• Outbreaks outside of Africa

–Serotypes 1-8• Limited geographical areas


African horse sickness (AHS) is caused by the African horse sickness

virus (AHSV), a non-enveloped, double-stranded RNA virus from the

family Reoviridae, genus Orbivirus. The AHS virus is comparable in

morphology and molecular structure to bluetongue virus (which is

considered the prototype virus of the Genus Orbivirus). There are nine

serotypes of the AHS virus, all of which are viscerotropic (having a

predilection for the abdominal and thoracic viscera). Serotype 9 is

widespread in endemic regions, while serotypes 1-8 are found only in

limited geographic areas. Serotype 9 has also been responsible for the

majority of AHS outbreaks outside of Africa. However serotype 4 caused

one outbreak in Spain and Portugal between 1987 and 1990.

[This photo shows an electron micrograph of Reoviridae from The

National Center for Biotechnology Information at

http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/60000000.htm]



Slide 5

African Horse Sickness Virus

• Inactivated by

–Heat (temps greater than 140oF)

–pH less than 6, or 12 or greater

–Acidic disinfectants

• Rapidly destroyed in carcasses that have undergone rigor mortis


The AHSV can be inactivated in the laboratory with formalin, β-

propriolactone, acetylethyleneimine derivatives or radiation. It is also

destroyed at a pH less than 6, or pH 12 or greater. Acidic disinfectants

such as 2% acetic or citric acid have been recommended for

decontamination when it is warranted. AHSV can survive in frozen meat,

but is inactivated at temperatures greater than 60oC) 140

oF. Optimum pH

for virus survival is pH 7-8.5. The virus is destroyed at a pH less than 6, or

pH 12 or greater; the virus is rapidly destroyed in carcasses that have

undergone rigor mortis due to pH fluctuations.

Slide 6

EPIDEMIOLOGY


Slide 7

Species Affected

• Equidae

–Horses, donkeys, mules

–Zebras

• Other

–Camels

–Dogs


The African horse sickness virus can infect horses, donkeys, mules, zebras,

camels and dogs. The most serious infections occur in horses and mules,

which appear to be accidental hosts. Zebras and donkeys rarely develop

serious clinical signs. Zebras, which are often asymptomatic, are thought

to be the natural reservoir hosts in most regions of Africa. Infections in

camels have been reported, but appear to be uncommon and asymptomatic.

[These photos show equids susceptible to African Horse Sickness. Top:

horse from P. Futoma, Iowa State University; Middle: mule from J.

Lascorz, http://commons.wikimedia.org; Bottom: zebra, from M.

Dezemery at http://www.flickr.com/photos/mdezemery/2461520029/]

Slide 8

Geographic Distribution

• Endemic in sub-Saharan Africa

• Outbreaks

–Southern and northern Africa

–Near and Middle East

–Spain and Portugal


African horse sickness is endemic to sub-Saharan central and east Africa.

The disease sometimes spreads to southern Africa and occasionally to

northern Africa. AHS epizootics became less common in southern Africa

during the latter half of the 20th century, possibly due to decreases in free-

ranging zebra populations. Outbreaks have been reported outside Africa, in

Egypt and other parts of the Middle East, as well as in Spain, Portugal,

Morocco, Pakistan and India.

[This map shows the distribution of most AHS cases from Government of

United Arab Emirates at

http://www.uae.gov.ae/uaeagricent/livestock/img/horse_Sickness1.jpg*]

*Link defunct as of 2010



Slide 9

OIE Disease Distribution Map


This map shows the reported disease distribution map for African horse

sickness for July-December 2010.

[Photo: World Animal Health Information Database, World Organization

for Animal Health (OIE).

http://web.oie.int/wahis/public.php?page=disease_status_map]

Slide 10

Incidence/Prevalence

• Seasonal– Late summer - early autumn

• Cyclic– Drought followed by heavy rains– Influences insect breeding

• Epizootics halted by– Frost– Lack of long-term vertebrate reservoir– Reduced numbers of vectors– Control measures

• Vaccination, vector abatement


African horse sickness has both a seasonal and an epizootic cyclical

incidence. The disease most commonly occurs in late summer to early

autumn, and after periods of drought followed by heavy rains. The warm,

moist conditions are optimal for vector breeding. Some authors speculate

that global warming could increase the risk for spread of arthropod-borne

diseases such as AHS. Epizootics of AHS outside the enzootic sub-

Saharan zone do not appear to be maintained for more than 2-3

consecutive years. Factors such as the absence of a long-term vertebrate

reservoir, reduced numbers of vectors, and efficient control measures

(vaccination and vector abatement) may play a role in preventing the

disease from becoming endemic in these areas. Outbreaks are abruptly

curtailed by severe frost. During the harsh winter months, the virus must

survive in an appropriate reservoir.

Slide 11

Morbidity/Mortality

• Varies with species, previous immunity, form of disease

• Mortality based on species

–Horse particularly susceptible


Species Mortality

Horses 50-95%

Mules 50%

European and Asian donkeys 5-10%

African donkeys and zebras Rare

Morbidity and mortality vary with the species of animal, previous

immunity, and the form of the disease. Horses are particularly susceptible

to the more severe forms of African horse sickness. The mixed and

pulmonary forms tend to predominate in susceptible horse populations,

and the mortality rate is usually 50% to 95%. In other species of Equidae,

African horse sickness is generally less severe. In mules, the mortality rate

is approximately 50%, and in European and Asian donkeys, 5% to 10%.

Death is rare in African donkeys and zebra. Animals that recover from

African horse sickness develop good immunity to the infecting serotype

and partial immunity to other serotypes.

Slide 12

Morbidity/Mortality

• Mortality based on form of disease


Disease Form Mortality

Pulmonary form Up to 95%

Cardiac form 50% or more

Mixed form 70-80%

Horsesickness fever Typically recover

The pulmonary form is nearly always fatal. The cardiac form of the

disease results in a mortality rate of 50% or higher. In the mixed form,

mortality ranges from 70% to greater than 80%. Horsesickness fever rarely

results in death.



Slide 13

TRANSMISSION


Slide 14

Transmission

• Not contagious

• Vector-borne: Culicoides spp.

–Culicoides imicola – principal vector

–C. bolitinos

–C. variipennis

–Other potential arthropods

• Viremia in Equidae

–Horses: 12 to 40 days

–Zebras, African donkeys: up to 6 weeksCenter for Food Security and Public Health, Iowa State University, 2011

African horse sickness is not a contagious disease; that is, it does not

spread directly from horse to horse. The virus is transmitted by the

arthropod-vector Culicoides (biting midges). The principal vector species

is Culicoides imicola ; however other Culicoides species (C. bolitinos or

C. variipennis, which is common in many parts of the United States)

should also be considered potential vectors. Transmission of AHS by other

arthropods is thought to be a very minor source of infection. Mosquitoes

may be potential biological vectors, while biting flies (e.g., Stomoxys and

Tabanus) may potentially serve as mechanical vectors. The viremia that

develops in Equidae species is high enough to infect competent vectors;

however, the length of viremia varies, lasting 12-40 days in horses and up

to 6 weeks in zebras and African donkeys.

[Photo: A Culicoides biting midge. Source: www.defra.gov.uk]

Slide 15

Culicoides spp.

• Biting midges, “punkies”, “no-see-ums”

– Extremely small ~1/8”

– Species identified by wing pattern

• Habitat

– Margins of water sources

• Life cycle: 2-6 weeks

– Eggs hatch in 2-10 days

• Females are bloodsucking

– Greatest biting activity dusk to dawn


Culicoides species, or biting midges, are flies in the family

Ceratopogonidae [Class: Insecta, Order: Diptera, Family:

Ceratopogonidae]. They have also been called “punkies”, and “no-see-

ums”. They are extremely small insects, typically measuring less than 1/8

inch and have distinctive wing patterns. Margins of streams and lakes,

mud holes, tree holes, salt marshes, tide pools, swamps, rice fields, and

runoff from dairy and feedlot pens are all habitats for Culicoides spp. The

insect’s life cycle ranges from 2-6 weeks, depending on the species and

environmental conditions. Eggs are usually deposited in masses of 25-300

in water, and hatch in about 3 days at 80oF. Only females feed on blood,

with the greatest time of biting activity occurring near dusk and around

dawn. Environmental temperature and moisture are the main factors

determining their prevalence in the environment.

[Photo: Culicoides (biting midge). Source: U.S. Department of

Agriculture]

Slide 16

ECONOMIC IMPORTANCE




Slide 17

History

• 1600: First recorded– Horses to southern Africa

• 1921: Sir Arnold Theiler– Described 7 major epizootics

in South Africa from 1780-1918

• 1959-61: Middle East– 1st outbreak outside Africa

• 1987-91: Spain, Portugal– Imported zebra reservoirs

– New Culicoides species


Historically, African horse sickness (AHS) was first recorded south of the

Sahara Desert in the mid-1600s with the introduction of horses to southern

Africa. In 1921, Sir Arnold Theiler (considered to be the father of

veterinary science in South Africa) described seven major epizootics

(a disease suddenly and temporarily affecting a large number of animals

over a large area) of AHS that occurred in South Africa between 1780-

1918. [Note: He also was responsible for developing an early vaccine for

the disease, which provided a foundation for future research leading to

effective preventive measures for this fatal disease of Equids]. In 1959-61,

the first documented outbreak of AHS out of its traditional enzootic region

of Africa occurred in the Middle East (Israel, Iran, Pakistan, Afghanistan,

India, Turkey, Iraq, Syria, Lebanon, Jordan, and Cyprus). During this

outbreak, as many as 300,000 animals died or were destroyed. India

reported a 90% mortality in Equidae involved. In 1987 Spain had an

outbreak of AHS, which later spread to Portugal. It was suspected that the

disease reached the country from subclinically infected zebras imported

from Namibia, Africa. [Note: Zebras show no clinical signs when infected

with the virus but can have viremia, and therefore be infectious for the

arthropod vector, for as long as 6 weeks]. During this outbreak, it was

found the virus was effectively spread by a non-traditional Culicoides

species, increasing the list of potential vectors capable of transmitting the

virus.

[Photo: Sir Arnold Theiler. Source: Gluck Equine Research Center,

Department of Veterinary Science, University of Kentucky.

http://www.ca.uky.edu/gluck/abouthoftheiler.asp; Data source:

http://www.cidrap.umn.edu/cidrap/content/biosecurity/ag-biosec/anim-

disease/ahs.html]

Slide 18

Economic Impact

• 1989: Portugal

–137 outbreaks

• 104 farms

–206 equines destroyed

–170,000 equinesvaccinated

–Cost $1.9 million


SPAIN

As an example of the economic impact the disease has had, especially in

naïve populations, lets look at the 1989 outbreak in Portugal. This was the

first time the disease was reported in this country, and followed outbreaks

occurring in Spain. Of the 137 outbreaks (on 104 farms), 206 equines died

(14%) or were destroyed (16%); 81.5% were horses, 10.7% were donkeys

and 7.8% were mules. An eradication campaign was initiated, including

the vaccination of all Portuguese equines (170,000 animals). Among those

animals vaccinated, 82 died or were euthanized due to suspected or

confirmed AHS. One year after ending vaccination, Portugal was declared

free of AHS. The estimated cost of the eradication campaign was US $1.9

million.

[This map shows the countries of Portugal and Spain. Source:

http://www.globalorganizationplanning.com/images/spain-map.gif; Data

source: Protas M, Boinas FS, Oliveira E, Sousa J, Rawlings F. African

horse sickness in Portugal: a successful eradication programme. Epidemiol

Infect. 1999 Oct; 123(2):337-46.]



Slide 19

U.S. Economic Impact

• U.S. Horse Industry (2007)

– Inventory: 4 million horses

–Sales: $2.0 billion

–Employment: 4.6 million Americans

• Risk factors

–Disease not in U.S. – naïve population

–Arthropod vector is in U.S.

–Outbreak would result in movement and trade restrictions


The potential impact of AHS in the U.S. could be substantial. In 2007, the

U.S. equine industry had an inventory of 4.0 million horses and 283

thousand mules, burros and donkeys, with a total value of sales of 2.0

billion dollars (USDA, National Agricultural Statistics Service, 2007

Census of Agriculture Database). Additionally, an estimated 4.6 million

Americans are involved in the industry (i.e., horse owners, service

providers, employees or volunteers). Since the disease has never occurred

in the Americas, our Equidae species are naïve and highly susceptible to

the virus. The U.S. has arthropod vectors potentially able to transmit

African horse sickness. Additionally, in the event of an outbreak of AHS

in the U.S., an emergency disease declaration and immediate ban on the

movement or trade of all Equidae species would be enacted. These factors

demonstrate the potential economic impact this disease could have if

introduced into the U.S.

Slide 20

AFRICAN HORSE SICKNESS IN ANIMALS


Slide 21

Incubation Period

• Experimental: 2-21 days

• Natural infection: 3-14 days


Disease Form Incubation Period

Peracute (pulmonary) form 3-5 days

Subacute (edematous or cardiac) form

7-14 days

Acute (mixed) form 5-7 days

Horsesickness fever 5-14 days

In experimental infections, the incubation period of AHS in Equidae has

been found to range from 2 to 21 days. In natural infections, the incubation

period appears to be approximately 3 to 5 days for the peracute

(pulmonary) form, 7 to 14 days for the subacute (edematous or cardiac)

form, 5 to 7 days for the acute (mixed) form and 5 to 14 days for

horsesickness fever.

Slide 22

Clinical Signs

• Four forms of the disease

–Peracute (pulmonary)

–Subacute edematous (cardiac)

–Acute (mixed)

–Horsesickness fever

• Symptomatic infections most common in horse and mules

• Zebras typically asymptomatic


As just mentioned, there are four different manifestations of African horse

sickness: the peracute (pulmonary) form, the subacute edematous (cardiac)

form, the acute (mixed) form, and horsesickness fever. Clinical signs are

characterized by damage to the respiratory and circulatory system as a

result of increased vascular permeability. Symptomatic infections occur

most often in horses and mules. The pulmonary and mixed forms usually

predominate in susceptible populations of horses. The pulmonary form is

also the most common form in dogs. The mildest form, horsesickness

fever, tends to be seen in horses with partial immunity, mules and

donkeys. This form can also occur in zebras, although most cases in this

species are asymptomatic.



Slide 23

Peracute - Pulmonary Form

• Acute fever

• Sudden, severerespiratory distress

• Dyspnea, tachypnea

• Profuse sweating

• Spasmodic coughing

• Frothy serofibrinous nasal exudate

• Rapid death (few hours)


Foam from the nares due

to pulmonary edema

The peracute or pulmonary form of African horse sickness usually begins

with an acute fever, followed by the sudden onset of severe respiratory

distress. Infected animals often stand with forelegs spread, head extended,

and nostrils fully dilated. Other clinical signs may include tachypnea,

forced expiration, profuse sweating, spasmodic coughing, and a frothy

serofibrinous nasal exudate. Dyspnea usually progresses rapidly, and the

animal often dies within a few hours after the respiratory signs appear.

Mortality for this form is nearly always fatal (near 95%).

[Photo: Abundant froth draining from the nostrils reflects severe

pulmonary edema. Source: Plum Island Animal Disease Center]

Slide 24

Subacute Edematous -Cardiac Form

• Edema–Supraorbital fossae,

eyelids

–Cheeks, lips, tongue, intermandibular space

–Neck, thorax, chest

–Not in lower legs

• If animal recovers, swellings subsideover 3-8 days


The subacute or cardiac form of African horse sickness usually begins

with a fever (102-106oF) that lasts for 3 to 6 days. Shortly before the fever

starts to subside, edematous swellings appear in the supraorbital fossae

(top photo) and eyelids (bottom photo). Swelling then spreads to involve

the cheeks, lips, tongue, intermandibular space, laryngeal region, and

sometimes the neck, shoulders and chest. It is important to note that no

edema of the lower legs is observed. If the animal recovers, the swellings

gradually subside over the next 3 to 8 days.

[Photo: (top) edematous swelling of the supraorbital fossae; (bottom)

palpebral conjunctivae. Source: USAHA ‘The Grey Book’]

Slide 25

Subacute - Cardiac Form

• Terminal stages

–Severe depression, colic, petechiae of conjunctivae and ventral tongue

• Death from cardiac failure

• Mortality 50% or higher

• Death within 4-8 days


Clinical signs seen in the terminal stage of the subacute/cardiac form of the

disease can include severe depression, colic, and petechiae under the

ventral surface of the tongue and in the conjunctivae. Death is typically

due to cardiac failure. The mortality rate for the subacute edematous or

cardiac form of AHS is usually 50% or higher, with death occurring 4 to 8

days after the onset of clinical signs.

Slide 26

Acute - Mixed Form

• Pulmonary and cardiac forms

• Cardiac signs usually subclinical

–Followed by severe respiratory distress

• Mild respiratory signs

–Followed by edema and death

• Diagnosed by necropsy

• Mortality 70-80%


In the acute or mixed form of African horse sickness, symptoms of both

the pulmonary and cardiac forms are seen. In most cases, the cardiac form

is subclinical and is followed by severe respiratory distress. Occasionally,

mild respiratory signs may be followed by edema and death from cardiac

failure. The mixed form of African horse sickness is rarely diagnosed

clinically, but is often seen at necropsy in horses and mules. The mortality

rate for the acute-mixed form varies from about 70% to greater than 80%.



Slide 27

Horsesickness Fever

• Mild clinical signs

• Characteristic fever (3 to 8 days)–Morning remission (undetectable)

–Afternoon exacerbation

• Other signs–Mild anorexia or depression

–Congested mucous membranes

– Increased heart rate

• Rarely fatalCenter for Food Security and Public Health, Iowa State University, 2011

In horsesickness fever, the clinical signs are mild. The characteristic fever

usually lasts for 3 to 8 days; morning remissions and afternoon

exacerbations are often seen. Other symptoms are generally mild and may

include mild anorexia or depression, edema of the supraorbital fossae,

congested mucous membranes and an increased heart rate. Animals almost

always recover from horse-sickness fever. This form of the disease is

rarely fatal.

Slide 28

Post Mortem Lesions

• Pulmonary form

–Severe, diffusepulmonary edema

–Hydrothorax

–Fluid in abdominal and thoracic cavity

–Enlarged endematous lymph nodes

–Hyperemia and petechial hemorrhages in intestines


In the pulmonary form of African horse sickness, interlobular edema of the

lungs and hydrothorax are the characteristic lesions. In the most acute

cases, frothy fluid flows from the nostrils and the cut surface of the lungs,

which are mottled red, noncollapsed and heavy. In more prolonged cases,

there may be extensive interstitial and subpleural edema, and hyperemia

may be less apparent. Fluid accumulation can occur in the abdominal and

thoracic cavities. Occasionally, extensive fluid accumulation may be noted

in the thoracic cavity (hydrothorax), with near normal appearance of the

lungs. The lymph nodes, particularly the nodes in the thoracic and

abdominal cavities, are usually enlarged and edematous. Less often, there

may be subcapsular hemorrhages in the spleen, congestion in the renal

cortex or gastric fundus, and edematous infiltration around the aorta and

trachea. The stomach mucosa may be hyperemic and edematous.

Hyperemia and petechial hemorrhages may also be apparent in the small

and large intestines and the pericardium may contain petechiae.

[Photo: Horse lung exhibiting severe interlobular edema. There are

petechiae on the pulmonary pleura and the splenic capsule. Source: Plum

Island Animal Disease Center]

Slide 29

Post Mortem Lesions

• Cardiac form

–Yellow gelatinous infiltrate

• Head, neck, shoulders

• Brisket, ventral abdomen, rump

–Hydropericardium

–Submucosal edema of cecum, large colon, rectum

• Mixed form

–Mixture of above findings


In the cardiac form, a yellow gelatinous infiltrate can be seen in the

subcutaneous and intermuscular fascia of the head, neck and shoulders,

and occasionally the brisket, ventral abdomen and rump.

Hydropericardium is common. The epicardium and endocardium often

contain petechial and ecchymotic hemorrhages. Lesions may also be found

in the gastrointestinal tract, resembling the pulmonary form. In addition,

prominent submucosal edema may be noted in the cecum, large colon and

rectum. Ascites can also be seen. In the cardiac form, the lungs are usually

normal or slightly engorged, and the thoracic cavity rarely contains excess

fluid. In the mixed form, the post-mortem lesions are a mixture of typical

findings from both the cardiac and pulmonary forms.

Slide 30

AHS in Other Species

• Dogs

– Ingestion of infected horse meat

–Not usually by insect bites

–No role in spread or maintenance

–Dogs usually have the pulmonary form

• Camels, zebras

– Inapparent infection


Experimentally, dogs have been found to be susceptible to the AHS virus.

Infection typically occurs following the consumption of virus-infected

horse meat. Canines are not thought to become naturally infected with

AHS through vector bites, and are also not considered important in the

spread or maintenance of the virus. It is generally accepted that dogs play

no role in the spread or maintenance of AHS because they do not develop

viremia sufficient to infect vectors. Camels and zebras can be inapparently

infected with AHS virus. In an Egyptian survey, antibodies were found in

sheep, goats, and buffaloes.



Slide 31

DIAGNOSIS AND TREATMENT


Slide 32

Differential Diagnosis

• Equine viral arteritis

• Equine infectious anemia

• Hendra virus infection

• Purpura hemorrhagica

• Equine piroplasmosis

• Equine encephalosis virus

• Anthrax

• ToxinsCenter for Food Security and Public Health, Iowa State University, 2011

The differential diagnosis includes equine viral arteritis, equine infectious

anemia, Hendra virus infection, purpura hemorrhagica and equine

piroplasmosis. In Africa, equine encephalosis virus, another orbivirus

transmitted by Culicoides, causes a syndrome resembling horsesickness

fever. Toxins, anthrax and other causes of sudden death, as well as

diseases that result in severe respiratory distress, should also be

considered.

Slide 33

Diagnosis

• Clinical signs

–Supraorbital swelling is characteristic

• History

–Prevalence or exposure to competent vectors

–Travel from enzootic area

• Laboratory tests - definitive diagnosis

• Serotype needed for control measures


African horse sickness should be suspected in Equidae demonstrating the

previously mentioned clinical signs. Supraorbital swellings are particularly

characteristic of this disease. Additionally, a history of prevalence or

exposure to competent vectors or of travel from an enzootic area can be

important factors. Tentative diagnosis of AHS may be obtained by

serology if blood is taken during the febrile stage; however, laboratory

confirmation is essential for definitive diagnosis, and serotype

determination will be important for control measures. Virus isolation and

identification may be done from a number of tissues; samples taken should

include small (2-4 g) sections of the spleen, lung, and lymph nodes.

Samples for virus isolation should be stored and transported at 4oC. AHS

viral antigens can be detected with enzyme-linked immunosorbent assays

(ELISAs), as well as with a reverse-transcription polymerase chain

reaction (RT-PCR), which can be particularly useful for rapid serotyping

of viral RNA. Currently there is no efficient treatment for African horse

sickness. Surviving Equidae develop solid immunity to the homologous

serotype but remain susceptible to heterologous serotypes. Vaccines have

been developed for all 9 serotypes of the virus, but are not currently

available in the U.S.

Slide 34

Laboratory Diagnosis

• Laboratory tests

–Virus isolation

–ELISA, RT-PCR

–Serology (tentative)

–Necropsy: spleen, lung, lymph node

• More than one test should be used

• AHSV does not cross-react with other known orbiviruses


African horse sickness can be diagnosed by isolating the virus or detecting

its nucleic acids or antigens. More than one test should be used to diagnose

an outbreak (particularly the index case) whenever possible. AHSV

antigens can be detected with enzyme-linked immunosorbent assays

(ELISAs). A reverse-transcription polymerase chain reaction (RT-PCR)

technique is used to detect viral RNA. A recently developed type-specific

RT-PCR assay can be used for rapid serotyping. Serology can also be used

to diagnose African horse sickness. Antibodies can be detected within 8 to

14 days after infection, and may persist for one to four years. The indirect

ELISA and complement fixation tests are the prescribed tests for

international trade. AHSV does not cross-react with other known

orbiviruses.



Slide 35

Sampling

• Before collecting or sending any samples, the proper authorities should be contacted.

• Samples should only be sent under secure conditions and to authorized laboratories to prevent the spread of the disease.


Before collecting or sending any samples from animals with a suspected

foreign animal disease, the proper authorities should be contacted.

Samples should only be sent under secure conditions and to authorized

laboratories to prevent the spread of the disease.

Slide 36

Samples To Collect

• For virus isolation

–Blood samples

–Necropsy samples

• Spleen, lung, lymph nodes

• Paired serum samples are recommended

• Store and transport samples at 39oF


In live animals, blood samples collected into anticoagulant should be taken

for virus isolation. Success is most likely if these samples are collected

early during the febrile stage. Necropsy samples for virus isolation should

include samples of the spleen, lung and lymph nodes. The samples for

virus isolation should be stored and transported at 4°C (39°F). Serum

should also be taken for serology. Paired serum samples are recommended,

and are particularly important in areas where the disease is endemic.

Slide 37

AFRICAN HORSE SICKNESS IN HUMANS


Slide 38

AHS in Humans

• No natural infection in humans

• Neurotropic vaccine strains

–Transnasal infection can lead to encephalitis or retinitis

• Handle modified live AHS vaccine strains with caution


There is no evidence that humans can become infected with field strains of

AHS virus through contact with infected animals, nor from working in

laboratories; however, it has been shown that certain neurotropic vaccine

strains may cause encephalitis and retinitis in humans following transnasal

infection. Modified live vaccine strains of AHS should be handled with

caution.

Slide 39

PREVENTION AND CONTROL




Slide 40

Recommended Actions

• IMMEDIATELY notify authorities

–OIE reportable disease

• In the U.S. notify

–Federal Area Veterinarian in Charge (AVIC) www.aphis.usda.gov/animal_health/area_offices/

–State Veterinarian www.usaha.org/Portals/6/StateAnimalHealthOfficials.pdf

• Quarantine premises


African horse sickness is reportable to the World Organization for Animal

Health (OIE). Disease notification requirements for OIE member nations

and import/export guidelines can be found in the OIE Terrestrial Animal

Health Code [http://www.oie.int/international-standard-setting/terrestrial-

code/access-online/].

If you suspect a case or outbreak of African horse sickness, contact your

state and/or federal veterinarian immediately and quarantine the premises.

If AHS is detected in a non-endemic country, a strict quarantine zone

should be established. Individual veterinarians who encounter a case of

African horse sickness should follow their national and/or local guidelines

for disease reporting and diagnostic testing.

Slide 41

Disinfection

• Disinfectants

–Sodium hypochlorite (bleach)

–2% acetic or citric acid

• Killed

–pH less than 6

–pH 12 or greater

• Rapidly destroyed in carcasses that have undergone rigor mortis


The AHS virus can be inactivated in the laboratory by formalin, -

propiolactone, acetyl-ethyleneimine derivatives, or radiation. Sodium

hypochlorite (bleach) is an effective disinfectant against the virus. The

virus is also destroyed at a pH less than 6 or greater than 12, so acidic

disinfectants, such as 2% acetic or citric acid have been recommended for

decontamination when warranted. Due to pH fluctuations, the AHS virus is

rapidly destroyed in carcasses that have undergone rigor mortis; however

the virus can survive in frozen meat, but is inactivated at temperatures

greater than 60˚C (140˚F).

Slide 42

Control

• Quarantine

–Equidae from endemic areas

• Asia, Africa, Mediterranean

–Minimum 60 days at point of entry

• Vector control and protection

– Insect repellants

–Stable in insect-proof housingfrom dusk to dawn


Horses cannot enter the US from an African horse sickness endemic

country unless they have been in an AHS-free country or area of the world

for at least 60 days. Upon entering the US, horses are then subject to the

regular 3 or 7 day quarantine period at the point of entry. If African horse

sickness is detected in a country where it is not endemic, a strict quarantine

zone and movement controls should be established. Euthanasia of infected

and exposed animals may be considered. Whenever possible, all Equidae

should be stabled in insect-proof housing. At a minimum, stabling from

dusk to dawn, the period when Culicoides are most active, is

recommended. Vector control measures such as modifications of

Culicoides breeding areas, insect repellents, and targeted applications of

insecticides or larvicides may also be useful.

Slide 43

Control

• Monitor temperature of all equids

– If febrile

• Euthanize or isolate in an insect-free stable until cause is determined

• Vaccination

– In endemic areas

–Surrounding protection zone

–Not available in the U.S.


Monitoring for fever may be helpful for the early detection of African

horse sickness. Each susceptible animal should have its temperature taken

regularly (optimally, twice daily). Those animals that develop a fever

should be kept in insect-free stables until the cause of the fever has been

established, or killed to prevent potential virus transmission to the vector.

In endemic areas, vaccination is strongly recommended for susceptible

Equidae. Additionally, areas around the affected area should vaccinate, as

well, to produce a surrounding protection zone.



Slide 44

Vaccination

• Attenuated live vaccine available

–Horses, mules, donkeys

–Not in U.S.

–Reassortment possible

–Teratogenic

• No killed or subunit vaccine available

• Recovering animals

– Lifelong immunity post-infection to the infecting serotype


Vaccines have been developed for the 9 serotypes of AHS virus.

Attenuated (monovalent and polyvalent) live (Vero cell) vaccines for use

in horses, mules, and donkeys are currently available in some countries

(but not in the U.S. at this time). These vaccines result in viremia, and the

viruses could theoretically reassort with an outbreak virus. Attenuated

vaccines may not be safe in AHS-free countries. They are also teratogenic.

No killed or subunit vaccines are currently manufactured commercially.

Animals that recover from the disease develop solid life-long immunity

against the infecting viral serotype.

Slide 45

Additional Resources

• World Organization for Animal Health (OIE)

– www.oie.int

• Center for Food Security and Public Health

– www.cfsph.iastate.edu

• USAHA Foreign Animal Diseases (“The Gray Book”)

– www.aphis.usda.gov/emergency_response/downloads/nahems/fad.pdf

• Center for Infectious Disease Research and Policy

– www.cidrap.umn.edu/cidrap/content/biosecurity/ag-biosec/anim-disease/ahs.htm

• African Horse Sickness Trust

– www.africanhorsesickness.co.za


For more information, see these listed resources.

References used for this presentation:

• Center for Food Security and Public Health (CFSPH). African horse

sickness. Technical Fact Sheet. 30 Nov 2006.

http://www.cfsph.iastate.edu/Factsheets/pdfs/african_horse_sickness.p

df

• U.S. Animal Health Association (USAHA). Foreign Animal Diseases,

7th edition. 2008. Guthrie, AJ. African Horse Sickness. p103-109.

www.aphis.usda.gov/emergency_response/downloads/nahems/fad.pdf

• Center for Infectious Disease Research and Policy (CIDRAP). African

horse sickness. 26 Sept 2004.

http://www.cidrap.umn.edu/cidrap/content/biosecurity/ag-biosec/anim-

disease/ahs.html

• U.S. Department of Agriculture, Animal and Plant Health Inspection

Service (USDA APHIS). Horse Reports and Highlights – African

Horsesickness.

http://www.aphis.usda.gov/animal_health/emergingissues/byspeciescat

egory/horse.shtml

Slide 46

Acknowledgments

Development of this presentation was made possible through grants provided to

the Center for Food Security and Public Health at Iowa State University, College of Veterinary Medicine from

the Centers for Disease Control and Prevention, the U.S. Department of Agriculture,

the Iowa Homeland Security and Emergency Management Division, and the

Multi-State Partnership for Security in Agriculture.

Authors: Glenda Dvorak, DVM, MPH, DACVPM; Anna Rovid Spickler, DVM, PhD

Reviewers: James A. Roth, DVM, PhD; Bindy Comito, BA; Katie Spaulding, BS; Meghan Blankenship, BS; Kerry Leedom Larson, DVM, MPH, PhD, DACVPM


Last reviewed: October 2011

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Etiology African Horse Sickness S Epidemiology African ... · African Horse Sickness ... virus (AHSV), a non-enveloped, double-stranded RNA virus from the family ... morphology and